This is not intended as medical advice and is not meant to replicate advice from your regular medical practitioner. In today’s low-carb interview, we discuss the physiology of cholesterol and all the roles that it plays within our body.
If you wish to find a low-carb doctor – CLICK HERE.
Today’s low-carb lesson – What is cholesterol? Is it all bad?
We have all heard the terms good cholesterol, bad cholesterol, triglycerides and particle sizes, but what does it all mean?
Today we clarify these terms and chat about cholesterol and how vital it is to our health and wellbeing.
What Is Cholesterol? Is it all bad?
Today we discuss:
- Why is cholesterol so vital to our health and well being?
- What are lipoproteins?
- What are HDL and LDL – are they good or bad?
- How important are particle sizes?
- What are triglycerides?
- Is cholesterol actually an anti-inflammatory?
- What are the risks of low-cholesterol?
- Who benefits from statins?
- Conclusion and what lipid panel should you ask from your doctor?
NOTE: There is a list of references at the end of this post for further reading.
What Is The Cholesterol Debate?
For decades we have been told that dietary cholesterol in food raises our blood cholesterol and raised blood cholesterol causes heart disease. But this is old and outdated science.
High blood cholesterol was thought to be a major risk factor for heart disease. This failed hypothesis is based on flawed and outdated research from 50 years ago.
I was once told by a GP, “if you are talking about good and bad cholesterol you’re 20 years out of date, if you’re talking about LDL still being an issue, you’re only 10 years out of date“.
The latest science heavily disputes the hypothesis that raised cholesterol causes heart disease, in fact, low cholesterol has been shown to have numerous detrimental effects, yet cholesterol is never spoken about in a positive light.
Most reports in the media, automatically link the terms cholesterol and heart disease together as if they are all one long word!
If you are talking about good and bad cholesterol you're 20 years out of date, if you're talking about LDL still being an issue, you're only 10 years out of date.Why is cholesterol so vital?
Cholesterol is so vital that our body is able to make (synthesise) the majority of what we require, only a small percentage actually comes from dietary cholesterol.
A lower intake from our food leads to increased cholesterol synthesis. And the converse is also true.
Cholesterol is required for numerous functions –
- Cholesterol is the basis of our sex hormones, steroid hormones, cortisol, oestrogen, and testosterone for example
- It is required for the synthesis of bile acid and Vitamin D (which is actually a hormone)
- Our cell membranes rely on cholesterol for both rigidity and fluidity
- Cholesterol is vital to normal brain function including learning and memory
What are lipoproteins?
We often talk about cholesterol, but it’s actually the lipoproteins that carry the cholesterol (the carriers) that we test. Cholesterol is a waxy substance that cannot be carried on the blood (a watery environment).
Cholesterol and triglycerides are lipids (fats) so cannot be transported through water-soluble areas such as blood, alone. They are packaged into a lipoprotein carrier. These lipoproteins carriers have a hydrophobic core and a hydrophilic outer membrane (figure below, image credit).
These lipoproteins are categorised into various types according to size and composition. (figure below).
Lipoproteins (the carriers) also transport a wide variety of hydrophobic compounds, nutrients and fat-soluble vitamins.
Different lipoproteins carry cholesterol but only ‘cholesterol is cholesterol’
Is there really good and bad cholesterol (carrier)?
Good and bad cholesterol are outdated terms. Some are more strongly associated with cardiovascular disease but remember from our Busting The Top 5 Nutrition Headlines lesson, association does not mean causation.
It’s like saying at every house fire there is always firemen. Do the firemen cause the house fires? No, they are just associated with house fires.
Are HDL and LDL good or bad?
HDL (high-density lipoproteins) was previously referred to as the “good” cholesterol. LDL (low-density lipoproteins) was previously referred to as the “bad” cholesterol. LDL particle size can range from 5 nm all the way up to 80nm. But to refer to good and bad cholesterol is outdated and doesn’t reflect the true picture of heart health and all the numerous factors that are involved.
LDL is very dynamic on a day to day basis. It changes immensely with fasting or feeding. When you fast, LDL can rise, and when eating a high-fat diet, LDL can drop.
LDL may be associated with heart disease, but does it cause it? Possibly not. It may be hinting at its involvement in the disease process, not the causation. There are populations and ages where higher LDL is associated with lower CVD mortality. But the TG/HDL ratio remains predictive independent of LDL.
These ideas and terminology of good or bad cholesterol, stem from the lipid hypothesis which is a static picture, but in fact, cholesterol is incredibly reactive and fluctuates day to day, meal to meal. So when we test and see numbers rise or fall, it is difficult to know whether these numbers are coming or going. So testing must be reviewed for each patient “in context”.
Further reading/watching: Dave Feldman – The Dynamic Influence of a High Fat Diet on Cholesterol Variability – CLICK HERE to watch.
Image credits: Dave Feldman
How important are particle sizes?
In your arteries it is the endothelium that is in contact with the blood, under pressure, small particle sizes may possibly infiltrate easier than larger particles. BUT the hypothesis cannot explain that HDL is even a smaller particle and does not have the same association nor do you find a gradient of particle sizes in arteries when autopsies are carried out.
To believe in the cholesterol/lipoprotein theory of heart disease, and invading via the vascular endothelium, you need to wave a magic wand? Lipoproteins cannot jump a 200 uM gap all the way to the intima-media junction.
What are triglycerides?
Triglycerides are a good reflection of your carbohydrate tolerance and carbohydrate intake. Clinicians often use triglycerides as a way to check ‘carb-creep’ due to triglycerides being very sensitive to carb intake.
The triglyceride/HDL ratio is a wonderful estimation of insulin resistance and heart disease.Levels can quite often drop dramatically over just s few days with the reduction of sugar and carbs from the diet. it is encouraging for patients to see such an immediate improvement.
Infections can also cause a transient rise “hypertriglyceridemia of infection” (probably via increased VLDL recruitment – see below).
The triglyceride/HDL ratio is a wonderful estimation of insulin resistance and heart disease.
Is cholesterol actually an anti-inflammatory?
Plaque formation is now recognized as an inflammatory process. There are many causes of inflammation and increased heart disease risk including smoking, stress, sugar and highly processed food. The most potent indicator of heart disease risk is insulin resistance, metabolic syndrome and hyperinsulinemia.
The hypothesis is that LDL may be one way we keep our own cells safe during times where levels of reactive oxygen species need to be higher for our own protection (it scavenges free-radicals).
Cholesterol plays an important part in our immune response, could this be why cholesterol is part of plaque formation? It is unclear.
What are the risks of low cholesterol?
As discussed, cholesterol is vital to our health and wellbeing. From infection control, memory, hormone production, libido and cell rigidity and fluidity. Cholesterol should stop being seen in a negative light and the dangers of low-cholesterol are not widely discussed.
Cholesterol is vital for memory, learning and brain function. Better memory and thinking are seen in over 85s despite high cholesterol. Declining cholesterol levels from midlife to late-life may better predict the onset of Alzheimer’s disease.
Cholesterol is vital for memory, learning and brain function. Better memory and thinking are seen in over 85s with high cholesterol.Cholesterol appears to protect us from acute infections (sepsis). For example, LDL prevents the virus that causes the common cold from entering through the LDL receptor and VLDL prevents the invasion of Malaria into the liver via the VLDL receptor.
The older you are, the associations suggest ‘the higher the better’ and you want to ensure your lipid ratios are correct.
Statins – who benefits?
Conventional thinking is that statins are a wonder drug, they have saved millions of lives and are especially effective in secondary prevention for people who have already had a heart attack. BUT is this correct?
In the BMJ, they looked at 6 studies for primary prevention (those who have not had a cardiovascular event) and secondary prevention (those who had already had a cardiovascular event). They discovered:
- Primary prevention – people died 5 days earlier or lived 19 days longer. The median increase in life expectancy = 3.2 days
- Secondary prevention – people died 10 days earlier or lived 27 days longer. The median increase in life expectancy = 4.1 days
The decision of whether to commence statin treatment should be a joint decision between yourself and your medical practitioner. Ultimately it is your decision to make and you must weigh up the possible benefit versus the side effects such as Type 2 diabetes and memory loss.
Further reading/watching: Malcolm Kendrick
Cholesterol – the conclusion
Top 3 Takeaways
- One single blood test should not be used for a lifetime of medication.
- Always do your own research. The decision whether to address a lipid panel, by drugs or by diet, should be done by mutual consent between you and your physician.
- A variety of blood tests, rather than one single test alone will give you a broader picture of your health.
Tests that reflect inflammation and metabolism are a better indicator of health and you must look at their TRENDS over time. Cholesterol testing is dynamic, not static and the numbers can be affected dramatically whether you have been fasting for too long, whether you have an infection, whether you live LCHF or the Standard American Diet (SAD) and stress, just to name a few. A test on Tuesday may be completely different than the same test taken on Friday depending on what you ate and how you slept.
Cholesterol alone does not give you a big enough picture. How is your blood pressure? HBA1C? Triglycerides? Inflammatory markers? Kidney function? Liver function? TG/HDL ratio? How do you look and feel?
If your HDL is high and your triglycerides are low, then this is an indicator of a strong metabolic status. Additional blood tests should be taken to confirm there aren’t any other bad indicators such as inflammation.
Raphi Sirtoli
Raphi Sirtoli can be found:
- Website – CLICK HERE
- Facebook page: CLICK HERE
- Twitter: CLICK HERE
Dave Feldman, as mentioned in our interview for the cholesterol code and the Feldman protocol. Website: CLICK HERE
You may also watch another low-carb lesson with myself and Raphi, “How to calculate macros. What are the insulin index and keto score?” CLICK HERE.
HOW TO START LOW-CARB
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There are all the resources you’ll ever need to learn how to start a low-carb diet or how to start a keto diet.
Further reading and references:
- High Low-Density Lipoprotein Cholesterol Inversely Relates to Dementia – “Our result indicates that a high level of LDL-C is inversely associated with dementia. High level of LDL-C may be considered as a potentially protective factor against cognition decline..”
- Study of the Use of Lipid Panels as a Marker of Insulin Resistance to Determine Cardiovascular Risk “Insulin resistance, as manifested by a high triglyceride/HDL-c ratio, was associated with adverse cardiovascular outcomes more than other lipid metrics, including LDL-c, which had little concordance. Physicians and patients should not overlook the triglyceride/HDL-c ratio.”
- Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target. “Anitschkow stated: ‘‘Lipids enter the arterial wall as compounds with protein fractions of blood plasma directly from arterial lumen’’ […] Remarkably, observations of early stages of human coronary atherosclerosis from the same group had already shown initial lipid deposition, not in the proximal but in the distal layers of DIT [diffuse intimal thickening], thereby bearing some contradictions to the hypothesis advanced by the authors”
- Early human atherosclerosis: accumulation of lipid and proteoglycans in intimal thickenings followed by macrophage infiltration. “In early human coronary atherosclerosis, fatty streaks develop via extracellular deposition of lipids associated with specific types of proteoglycans in the outer layer of preexisting DIT [diffuse intimal thickening]. As the amount of the lipid increases in fatty streaks, macrophages infiltrate toward the deposited lipid to form PIT [pathologic intimal thickening] with foam cells”
- Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines (Sachdeva et al. 2009)
“In a large cohort of patients hospitalized with CAD, almost half have admission LDL levels <100 mg/dL. More than half the patients have admission HDL levels <40 mg/dL, whereas <10% have HDL > or =60 mg/dL” - BMJ rapid response: Statins for the primary prevention of cardiovascular disease (Cait S.E. O’Sullivan, clinical pharmacist, 2014)
“Given the less than complete picture of the net benefit of statins when prescribed for primary prevention we do hope clinicians will choose not to use the “Tips for patients” sheet to incompletely inform patients and that they will welcome tough questions raised when patients are advised that they must take a statin “every day and for the foreseeable future” - Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein (Ridker et al. 2008, Jupiter study).
- Myocardial infarction (MI): Placebo (68 MIs & 6 deaths) vs Statin (31 MIs & 9 deaths)
- Stroke: Placebo (64 strokes & 6 deaths) vs Statin (33 strokes & 3 deaths)
- Stroke + MI: Placebo (12 deaths from strokes + MIs) vs Statin (12 deaths from stroke + MIs)
- The effect of statins on average survival in randomised trials, an analysis of end point postponement (Kristensen et al. 2015). “6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively”
- LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature (Ravnskov et al. 2018). “Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations”.
- High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study (Walladius et al. 2001). ApoB alone is a worse predictor of fatal MIs than the ApoB/Apo-A1 ratio.
- Interrelation between angiographic severity of coronary artery disease and plasma levels of insulin, C-peptide and plasminogen activator inhibitor-1 (Negri et al. 1993). “These findings support that hypothesis and suggest that insulin secretion may be an index of the severity of CAD. Because a direct effect of insulin on the cells that synthesize PAI-1 has been shown, the present data further indicate that the effect of insulin on fibrinolysis may be another way by which hyperinsulinemia accelerates atherogenesis.”
- Low-density lipoprotein subfractions and the long-term risk of ischemic heart disease in men: 13-year follow-up data from the Québec Cardiovascular Study (St.Pierre et al. 2005). ApoB appears significant in a hyperinsulinemic context (not as a stand-alone marker)
- Determinants of serum triglycerides and high-density lipoprotein cholesterol in traditional Trobriand Islanders: the Kitava Study (Lindeberg et al. 2003). Kitavans had very low rates of CVD but had high levels of apoB. This is a ‘black swan’ to the lipoprotein gradient hypothesis of CVD.
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